Helicobacter pylori Seropositivity in Patients with Acute Coronary Syndromes

Abstract

The aim of this study was to investigate the seroprevalence of Helicobacter pylori (HP) in patients with coronary atherosclerosis and acute coronary syndromes. We enrolled 152 patients (group I, 73 patients with acute coronary syndrome; group II, 79 patients with chronic stable angina) and 22 control subjects. An enzyme-linked immunosorbent assay for immunoglobulin (Ig) G test for HP diagnosis was used on all enrolled subjects. C-reactive protein (CRP) was also measured in all patients as an inflammatory marker. Seropositivity rates for HP were significantly higher in patients with coronary artery disease than in controls (80.2% versus 54.5%; P < 0.05). Although CRP level was significantly higher in group I than in group II (1.72 +/- 2.89 mg/dl versus 0.53 +/- 0.63 mg/dl, P < 0.0001), HP infection rates were similar between groups (86.3% versus 74.6%, P > 0.05). Infection with HP may influence atherogenesis through low-grade, persistent inflammatory stimulation. However, our data show evidence of increased systemic inflammation in patients with acute coronary syndrome, which was unrelated to an increased HP seropositivity.

Lack of Association Between Helicobacter Pylori's Virulence and Increased Serum C-Reactive Protein Levels in Functional Dyspeptic Patients

“…Although it was observed an inverse relation between H. pylori infection and serum albumin, the bacteria presence was unrelated to C-reactive protein and the leukocyte count, regardless of CagA status (4) . Such result was also reported in several studies that showed no impact of H. pylori's infection in systemic markers of inflammation (13,15,36,38) . CagA is the most extensively investigated virulence factor of H. pylori being encoded by cytotoxin-associated genes pathogenicity island (cagPAI) (3) .…”

Infections and autoimmunity – friends or foes?

“…Several epidemiological studies have suggested an association between H. pylori seropositivity and atherosclerosis [43] [44]. The Th1 immune response against heat shock protein 60 (HSP60) derived from pathogens is thought to be a proatherogenic process and was related to the progression of atherosclerosis in a hyperlipidemic mouse model [45].…”

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

“…Substantial biological data implicate inflammatory pathways in the onset of early atherogenesis, progression of the lesions and thrombotic complications associated with this disease. Clinical investigations have confirmed correlations between circulating markers of inflammation, such as C-reactive protein (CRP) 28,71,72) , tumor necrosis factor (TNF) 73,74) , interleukin (IL)-6 71,75) and IL-18 76,77) , and the occurrence of atherosclerosis and its cerebrovascular or cardiovascular events. In addition, growing evidence suggests that H. pylori infection, accompanied by persistent low-grade systematic inflammation, contributes to the risk of atherosclerosis by stimulating the production of proinflammatory cytokines, such as CRP 78,79) , IL-6 80) , and IL-18 81) , all of which are predictors of atherosclerosis.…”